YKL-40 as a Novel Factor Associated with Inflammation and Catabolic Mechanisms in Osteoarthritic JointsReportar como inadecuado




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Mediators of InflammationVolume 2014 2014, Article ID 215140, 7 pages

Research Article

The Immunopharmacology Research Group, University of Tampere School of Medicine and Tampere University Hospital, 33014 Tampere, Finland

Coxa Hospital for Joint Replacement, P.O. Box 652, 33101 Tampere, Finland

Received 19 June 2014; Accepted 4 July 2014; Published 15 July 2014

Academic Editor: Luca Cantarini

Copyright © 2014 Tuija Väänänen et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

YKL-40 is associated with tissue injury and inflammation, and consequently to diseases in which these mechanisms lead to tissue degradation, for example, asthma and rheumatoid arthritis. The purpose of the present study was to investigate if YKL-40 is also a significant factor in osteoarthritis OA by assessing associations of YKL-40 with mediators related to the pathogenesis of OA: cartilage destructing matrix metalloproteinases MMPs and proinflammatory cytokines interleukin-6 IL-6 and interleukin-17 IL-17. Cartilage, synovial fluid SF, and plasma samples were obtained from 100 OA patients undergoing total knee replacement surgery. SF levels of YKL-40 1027.9 ± 78.3 ng-mL were considerably higher than plasma levels 67.2 ± 4.5 ng-mL and correlated with YKL-40 released from cartilage samples obtained from the same patients , , indicating that YKL-40 is produced by OA cartilage. Interestingly, YKL-40 concentrations in OA SF correlated positively with MMP-1 , , MMP-3 , , IL-6 , , and IL-17 , levels. Moreover, IL-6 and IL-17 enhanced YKL-40 production in human primary chondrocyte cultures. The present study introduces YKL-40 as a cartilage-derived factor associated with mediators of inflammation and cartilage destruction involved in the pathogenesis of OA.





Autor: Tuija Väänänen, Anna Koskinen, Erja-Leena Paukkeri, Mari Hämäläinen, Teemu Moilanen, Eeva Moilanen, and Katriina Vuolt

Fuente: https://www.hindawi.com/



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